The role of carbon dioxide and atmospheric air in double-contrast barium enema

Background Patient discomfort 0–24 h after double-contrast barium enema (DCBE) was investigated in two ways.Methods In part 1, 139 patients, not previously informed, were contacted by telephone to assess symptom rates without bias. In part 2, designed as a prospective randomized double-blind trial, the effect of carbon dioxide (CO₂) as an insufflating gas was compared with conventional atmospheric air (AA).Results Part 1: 10% experienced severe abdominal pain, and 18% severe abdominal distention. Part 2: Low discomfort rates were found for both severe pain (7% for AA vs. 2% for CO₂) and severe distention (13% for AA vs. 8% for CO₂); the differences were not significant. In both parts of the study, female patients with a history of abdominal discomfort of colon irritabile type were significantly overrepresented in the severely symptomatic groups. Equal numbers of patients experiencing severe abdominal distention for the first time were found in both the AA and CO₂ groups, ruling out AA as the sole cause of these symptoms.Conclusion Abdominal post-DCBE discomfort seems to be less frequent than previously reported and is not effectively eliminated by CO₂. We still find the use of AA in DCBEs justified.     

复合营养素提高机体高原急性缺氧耐力的研究

用两种复合营养制剂对90 名空运入藏战士进行了提高机体急性缺氧耐力的研究。PWC170机能试验、血压、血乳酸、血丙酮酸含量测定及急性高原反应症状调查结果表明, 两种复合营养制剂都有助于维持正常的心血管功能、增强组织有氧代谢和减轻急性高原反应症状, 因此能有效的提高机体急性缺氧耐力, 其中以Ⅱ号配方的作用更佳     

红景天提取物的制备及其抗缺氧抗疲劳作用

目的 :探讨红景天对提高缺氧耐力和劳动能力的机理 ,为提高运动能力和在缺氧环境下的工作能力提出防护办法。方法 :对红景天提取物进行初步纯化 ,以小鼠常压缺氧和力竭游泳时间作为耐氧能力和劳动能力指标 ,对动物服药前后的体重变化进行考察。结果 :红景天可明显提高动物的缺氧耐力和劳动能力 ,减轻体重。提示服用红景天可以作为缺氧环境下提高工作能力的有效措施 ,并可作为舰艇长航人员防止体力耐力下降、肥胖人员减肥、轻量级运动员提高运动能力的保健药物。     

苯妥英钠对小鼠急性低压缺氧学习记忆障碍的影响

将40只体重20～24g昆明种小鼠随机分为4组,在建立急性低压缺氧导致小鼠学习记忆障碍模型基础上,采用跳台和避暗两种实验方法观察了苯妥英钠(DPH)对小鼠学习记忆障碍的影响.结果表明,急性低压缺氧(8km,停留30min)可导致小鼠学习记忆障碍;灌服DPH(40mg/kg)有一定的防治作用.     

模拟飞行缺氧与吸氧对小鼠脏器自由基代谢的影响

目的 观察了两种模拟飞行条件（１５００ｍ轻度低压缺氧和５５００ｍ中度低压吸氧重复暴露下小鼠多脏器自由基代谢变化的特点。方法 昆明种小鼠６０只,随机分为６组（ｎ＝１０）进行缺氧与吸氧实验,实验完毕后,取小鼠尾血做血常规检查。次日,将小鼠断头处死,取脑、心、肺、肝、肾制备匀浆,测定丙二醛（ＭＤＡ）含量和超氧化物歧化酶（ＳＯＤ）活性。结果 １５００ｍ轻度低压缺氧重复暴露８ｗｋ使肺ＭＤＡ含量显著增高,提示     

Dexamethasone effects on cerebral protein synthesis prior to and following hypoxia-ischemia in immature rat

We hypothesized that the neuroprotection against cerebral hypoxic-ischemic damage observed with dexamethasone treatment in immature rats is related to a change in cerebral protein synthesis. Six-day-old Wistar rats were injected with either vehicle (10 ml/kg) or dexamethasone (0.1 mg/kg) 24 h prior to cerebral hypoxia-ischemia. Local cerebral protein synthesis (incorporation of 14C-leucine into proteins) was measured in 7-day-old rats during normoxia, during hypoxia-ischemia, and after hypoxia-ischemia which was produced with right carotid artery ligation and 2-h exposure to 8% O2. In normoxic controls, cerebral protein synthesis was similar in dexamethasone and vehicle-treated animals. During hypoxia-ischemia, local cerebral protein synthesis decreased markedly (p < 0.0001) in ischemic regions ipsilateral to the occlusion, irrespective of treatment. After hypoxia-ischemia, protein synthesis declined even further in vehicle-treated animals. Reductions in protein synthesis were substantially more severe in vehicle- than dexamethasone-treated animals, particularly after hypoxia-ischemia (p < 0.0001). Thus, neuroprotection with dexamethasone is not related to a reduction in basal levels of cerebral protein synthesis, but is associated with an improved protein synthesis during and following hypoxia-ischemia.     

Adenosine inhibits L-type Ca2+ current and catecholamine release in the rabbit carotid body chemoreceptor cells

In an in vitro preparation of the intact carotid body (CB) of the rabbit, adenosine (100 microM) inhibited hypoxia-induced catecholamine release by 25%. The specific A1 antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 1 microM) prevented the inhibition and increased the response to hypoxia further. In isolated chemoreceptor cells from the same species, adenosine inhibited voltage-dependent Ca2+ currents by 29% at 1 microM (concentration producing half-maximal inhibition, IC50 = 50 nM). This inhibition was mimicked by R(-)N6-(2-phenylisopropyl)-adenosine and 2-chloroadenosine (1 microM), two purinergic agonists poorly active at the intracellular ('P') site, and persisted in the presence of dipyridamole (a blocker of adenosine uptake; 1 microM) and was fully inhibited by 8-phenyltheophylline (10 microM). The A1 antagonists DPCPX (10 microM) and 8-cyclopentyl-1,3-dimethylxantine (0.1 microM) inhibited the effect of adenosine by 93% (IC50 = 0.14 microM) and 59%, respectively. The inhibition of the Ca2+ current (I(Ca)) was reduced by nisoldipine (an L-type Ca2+ channel antagonist) by nearly 50%, and was unaltered by omega-conotoxin GVIA, a blocker of N-type Ca2+ channels. Adenosine did not affect the voltage-dependent Na+ current (I(Na)) or K+ current (I(K)). We conclude that adenosine A1 receptors are located in chemoreceptor cells and mediate the inhibition of L-type Ca2+ channels and thereby the release of catecholamines produced by hypoxia. The data also indicate that endogenous adenosine acts as a physiological negative modulator of the chemoreceptor cell function. The previously reported excitatory action of adenosine on the activity of the sensory nerve of the CB is discussed in terms of a balance between the inhibition mediated by A1 receptors and the excitation mediated by A2 receptors.     

Hypoxia induces differential changes of dopamine metabolism in mature and immature mesencephalic and diencephalic cell cultures

Summary. Perinatal hypoxia is known as a high risk factor for the development of long-lasting abnormalities in dopaminergic system. The early developmental alterations of dopamine (DA) metabolism induced by hypoxia could contribute to these abnormalities. To understand the hypoxia-induced changes of intra- and extracellular dopamine levels and its main metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), in immature dopaminergic neurons, we compared these changes in rat mesencephalic and diencephalic cell cultures on day in vitro (DIV) 2 (immature cells), DIV 8 and DIV 13 (mature cells). Cell cultures were exposed to an oxygen-free gas mixture in a Billups chamber for 2–4 hours. Mature cell cultures responded to hypoxia with an increase of DA levels in the cells and in the medium during the first 45 min (by an average of 57 and 114% respectively). Thereafter, DA levels decreased, and returned to the baseline within the next 30 min. The cellular DA levels continued to decrease up to 15% of the baseline during 255 min hypoxia whereas the extracellular DA content stabilized at the prehypoxic levels. Immature cell cultures (DIV 2) in contrast to mature ones, were unable to maintain normal extracellular DA levels during hypoxia and showed a decrease of the cellular and extracellular levels to 50% of the prehypoxic levels. DOPAC and HVA changes mimick, however, at a lower level, the pattern of DA changes during the exposure to hypoxia. In principle, in the diencephalic cell culture similar effects of hypoxia exposure on the investigated parameters were found (studied during 0–120 min). The present study demonstrates that mature and immature dopaminergic cells differ in the regulation of the extra- and intracellular DA levels during hypoxia. In immature cells the low synthetic capacity of tyrosine hydroxylase and the deficient capacities of the transport and storage processes result in decreased extracellular DA levels. This could be an important factor for the long-term modulation of the expression of tyrosine hydroxylase and subsequent long-term behavioral and/or neurological abnormalities induced by perinatal hypoxia. Received June 8, 1998; accepted July 21, 1998     

Cytoskeleton mediates inhibition of the fast Na+ current in respiratory brainstem neurons during hypoxia

Whole-cell Na+ currents (INa) were recorded in inspiratory neurons in a medullary slice preparation from neonatal mouse that contains the functional respiratory network. Hypoxia and metabolic poisoning with KCN rapidly inhibited INa by reducing the number of Na+ channels available for opening during depolarization. Application of agents specific for G-proteins, protein kinase C and A, intracellular Ca2+ and pH did not prevent the hypoxic inhibition of INa. The effects of hypo-osmolarity and hypoxia were additive, whereas hyperosmolarity partially prevented a subsequent hypoxic inhibition of INa. Cytochalasin B and colchicine decreased, and taxol or phalloidin increased INa and reduced its hypoxic inhibition. We conclude that cytoskeleton rearrangements during hypoxia are responsible for suppression of a fast INa in brainstem respiratory neurons, which could be mediated by the uncoupling of channel inactivation gates from cytoskeletal elements.     

新生儿缺氧缺血性脑病24例临床分析

目的 为了早期预防、及时诊疗,减少新生儿缺氧缺血性脑病(HIE)的死亡和病残率。方法：加强国产期保健,防治新生儿窒息,加强对胎儿的监护,提高产科技术,适当放宽剖腹产手术指征。在治疗HIE应采取综合疗法,其中最基本的措施是维持机体内环境稳定,维护各脏器正常功能。应用丽珠赛乐(国产脑活素)及胞二磷胆碱。结果：HIE患儿疗效提高,使轻、中度病例不产生神经后遗症。结论：应及早使用脑细胞代谢激活剂治疗,尽快使受损神经细胞恢复代谢功能,避免神经细胞死亡及产生后遗症。